The effects of nutrition, oxidation, and other environmental factors (light intensity or darkness) on the incidence and progress of posterior subcapsular opacities (PSO) associated with retinal degeneration are being studied in Royal College of Surgeons (RCS) rats, in which rod photoreceptor outer segment debris accumulates secondary to a phagocytic defect in the retinal pigmented epithelium. Evidence has been obtained that oxidative changes in polyunsaturated fatty acids in the debris lead to water-soluble toxic aldehydes that can be detected in the vitreous, and are toxic to lens cells and their membranes. Pink-eyed RCS dystrophic rats fed a natural ingredient diet (NIH-07) are highly sensitive to retinal light damage, beginning at light levels as low as 1-4 footcandles, and 27% of such rats develop mature cataracts by 7-12 months. Increased intensity of light (either cyclic or constant) increased the percentage of rats with mature cataracts, while dark rearing from birth prevented the PSO and mature cataracts. Recently, we have found that a purified diet (AIN-76A) fortified with 0.4% beta-carotene + 0.01% BHT also prevented the PSO and mature cataracts. Rhodopsin bleaching appears to be essential for retinal light damage and for initiation of the PSO. A hypothesis has been developed that would explain these findings. It depends upon the known capacity of retinaldehyde to act as a photosensitizer to generate singlet oxygen, an extremely energetic oxidant for polyunsaturated lipids, as well as proteins. Darkness would prevent release of retinaldehyde, while beta-carotene is a direct physical quencher of singlet oxygen, and BHT a highly efficient scavenger for secondary oxidized products. Principles established with the RCS rat model may have significance for slowing or preventing human PSO and mature cataracts, such as those seen in retinitis pigmentosa.